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71 Cards in this Set
- Front
- Back
anaplasia
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an exaggerated form of dysplasia that can be observed in malignant cells that includes varying degrees of cytologic and nuclear atypia, alteration in the shape and size of the cell and/or nucleus, loss of cell orientation, and abnormal mitoses
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anthracosis
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accumulation in the lungs from inhaled smoke or coal dust; miner’s lung
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apoptosis
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a distinctive form of cell death that involves individual cells or small clusters of; active, energy-dependent process under strict regulatory control that does not illicit an inflammatory response
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apoptotic body
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small, membrane-bound segment of a cell that results from apoptosis; phagocytized by macrophages via receptor binding
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autolysis
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cellular destruction caused by endogenous enzymes
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autophagic vacuole
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formed by fusion of a lysosome with a cytoplasmic structure to digest intracellular material
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autophagy
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digestion of cellular material by enzymes of the same cell
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caspaces
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a family of intracellular proteolytic enzymes that mediate the apoptotic process present within the cytosol in their inactive form (procaspaces)
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catabolism
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destructive metabolism in which complex materials are broken down to release energy
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chromatin
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the finely-dispersed state in which DNA can be found in the nucleus of a resting (non-dividing) cell
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crepitation
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– to make a crackling sound due to air bubbles beneath the surface of the skin
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cytokine
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regulatory protein released by cells of the immune system that act as intercellular mediators of the immune response
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cytoskeleton
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an integral part of the cytoplasm that allows for cell motility and maintains cell structure, consisting of microfilaments, cell-type specific intermediate filaments, and microtubules
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cytosol
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the amorphous ground substance of the cytoplasm consisting of water, nutrients, carbohydrates, lipids, and proteins; also the location of cellular organelles
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etiology
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cause or origin of a disease
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ferritin
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ferric iron-apoferritin protein complex involved in normal iron absorption and storage
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frostbite
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damaged vascular endothelium increases vascular permeability, leading to edema and blister formation
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heterolysis
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cellular destruction caused by exogenous enzymes
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homeostasis
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ability to maintain internal equilibrium by adjusting physiological processes
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heterophagy
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digestion within a cell of a substance taken into the cell by phagocytosis from the outside environment
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karyolysis
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chromatin dissolution, definitive morphologic evidence of irreversible cell injury and death
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karyorrhexis
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chromatin fragmentation, definitive morphologic evidence of irreversible cell injury and death
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parenchyma
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generally composed of epithelial cells, this tissue is the distinctive (often functional) cells of an organ
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pathogenesis
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the development of a diseased condition
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psammoma body
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small, concentrically laminated sphere of calcium, representing a calcium deposit
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pyknosis
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dense chromatin condensation, definitive morphologic evidence of irreversible cell injury and death
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residual body
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remnant of material that lysosomes are unable to digest found in the cytoplasm
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stroma
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generally composed of mesenchymal connective tissue cells, this tissue provides the structural framework of an organ
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hydropic change
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an exaggerated form of cellular swelling in which ER looks like water vacuoles; surrounding microvasculature may be compressed and add to cellular injury
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steatosis
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is an absolute increase in lipids within parenchymal cells, usually in the liver but sometimes in the heart or kidney; different from fatty ingrowth
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what is lipofuscin associated with?
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brown atrophy of heart and liver
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what is the clinical significance of hemosiderin?
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abnormal breakdown of RBCs
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compare and contrast hemochromatosis and hemosiderosis
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hemosiderosis - hemosiderin is present in excessive amounts, result of chronic hemolysis of RBCs, found in heart, liver, pancreas, skin
hemochromatosis - severe metabolic disorder, defect in normal iron metabolism, masssive iron depositions in heart, liver, pancreas, and skin that leads to cirrhosis, diabetes mellitus, bronze skin discoloration, and heart failure |
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what causes coagulative necrosis
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inadequate cell oxygenation, often due to ischemia
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what causes dry gangrene
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ischemic coagulative necrosis of skin and subcutaneous tissues of extremities
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what causes wet gangrene
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tissue hypoxia secondary to ischemia
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what causes liquefactive necrosis
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bacterial infections attract neutrophils, resulting in abscesses; ischemic destruction of brain tissue
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what causes caseous necrosis
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infectious diseases with mycobacteria and fungi
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what causes enzymatic fat necrosis
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pancreatic enzymes (lipases) act on fat cells to convert triglycerides to free FAs that complex with calcium to form calcium soaps
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what causes traumatic fat necrosis
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traumatic rupture of fat cells followed by phagocytosis of lipid material
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what causes fibrinoid necrosis
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deposition of immunoglobulins, fibrinogen, and complement in blood vessel walls
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what are some pro-apoptotic factors
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include TNFα, glucocorticoids, chemotherapeutic drugs, free radicals, and UV radiation
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what are some anti-apoptotic factors
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growth factors, sex steroids, and the EB virus.
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what are the factors in the extrinsic activation of caspase activity (apoptosis)
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FAS protein, TNF (on cell surface), initiator procaspace - procaspace 8
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what are the factors in the intrinsic activation of caspace activity (apoptosis)
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mitochondrial membranes, Bcl-2 proteins, Bcl-x (both decrease) Bax and Bak both increase, cytochrome C is released, binds to Apaf-1, activates initiator procaspace 9
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what is a full thickness burn?
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destroy the epidermis as well as the underlying dermis and dermal appendages, so reepithelialization cannot occur. Healing takes a long time, must occur from the outside edges, and there is an increased risk of infection
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what is a partial thickness burn
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destroy the epidermis, but leave the basal epithelium or at least some of the dermal appendages intact, so epithelial cells can be regenerated
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abrasion
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friction; crushing
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avulsion
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tearing away of body parts
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contusion
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distruption of blood vessls produced by blunt force, bruising
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laceration
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tearing of tissue resulting from excessive stretching, leaves nerves and small vessels intact
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incision
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cut produced by small instrument
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puncture
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piercing or penetration of tissue caused by sharp instrument
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dystrophic calcifications
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occur in degenerating or necrotic tissue of patients with normal serum calcium levels. Calcium accumulates in irreparably damaged mitochondria; extracellular calcium deposits also develop by using membrane-bound vesicles for propagation
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metastatic calcification
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the deposition of calcium in normal tissues of patients with high serum calcium levels; this tends to occur in tissues with relatively alkaline pH, such as the cornea, lungs, stomach, and blood vessels.
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anasarca
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diffuse, generalized edema throughout the body
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ascites
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accumulation of fluid within the peritoneal cavity due to increased hydrostatic pressure within the portal venous system
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brown induration
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gross appearance of the lungs due to fibrous thickening of alveolar walls
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cyanosis
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bluish discoloration of tissue
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diapedesis
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the movement of blood cells through intact capillary walls into surrounding tissue
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dyspnea
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difficulty breathing, often associated with lung or heart disease
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edema
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accumulation of excess fluid in cells or tissues; generally starts in loose connective tissue, so one of the first signs of edema is puffiness around the eye
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effusion
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seeping of fluid into a body cavity or tissue
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nutmeg liver
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fatty change of peripheral periportal hepatocytes resulting in a mottled red-brown and yellow-tan gross appearance of the liver
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orthopnea
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discomfort in breathing when laying down; this is measured by the number of pillows required for a patient to breathe and sleep at night
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rales/crackles
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abnormal respiratory sounds associated with pulmonary edema
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what happens when there is an increase in total body Na+
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increased osmotic pressure of interstitial fluid → generalized edema
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what happens when there is decreased serum albumin
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decreased oncotic pressure of plasma protein → generalized edema
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what happens when there is interference with or obstruction to venous blood flow
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→ increased hydrostatic pressure of intravascular fluid → localized edema
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transudate
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is a protein-poor (<3 gm/dL) pale, clear yellow fluid that develops from imbalances in the normal hemodynamic forces. It’s often seen with CHF, liver disease, renal disease, and GI disorders
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exudate
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s a protein-rich (>3gm/dL) cloudy yellow fluid that develops from endothelial damage and alteration of vascular permeability. It’s often seen with inflammatory or immunologic disorders.
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